ELECTROPHYSIOLOGICAL DEMONSTRATION OF N-METHYL-D-ASPARTATE RECEPTORS AT THE AFFERENT SYNAPSE OF CATFISH ELECTRORECEPTOR ORGANS

Citation
Gn. Andrianov et al., ELECTROPHYSIOLOGICAL DEMONSTRATION OF N-METHYL-D-ASPARTATE RECEPTORS AT THE AFFERENT SYNAPSE OF CATFISH ELECTRORECEPTOR ORGANS, Neuroscience, 79(4), 1997, pp. 1231-1237
Citations number
19
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03064522
Volume
79
Issue
4
Year of publication
1997
Pages
1231 - 1237
Database
ISI
SICI code
0306-4522(1997)79:4<1231:EDONRA>2.0.ZU;2-D
Abstract
An excitatory amino acid, most probably L-glutamate, acts as a neurotr ansmitter at the receptor cell-afferent fibre synapses in the ampullar y electroreceptor organs of the freshwater catfish Ictalurus nebulosus . In the present study, we have used an electrophysiological approach to investigate the presence of N-methyl-D-aspartate receptors at this level. N-Methyl-D-aspartate, dissolved in an Mg2+-containing (normal) solution, had no effect on afferent activity, not even at 5 mM. Howeve r, addition of 5 mM N-methyl-D-aspartate to an Mg2+-free solution evok ed an enduring increase in firing rate. The application of N-methyl-D- aspartate combined with electrical sine wave stimulation produced a fi ring increase in the primary afferents, even in the presence of Mg2+ ( 1.5 mM). Glycine (0.01-0.001 mM) significantly potentiated the N-methy l-D-aspartate responses. Addition of antagonists of the actions of N-m ethyl-D-aspartate, 7-chlorokynurenic acid, DL-2-amino-5-phosphonovaler ic acid and ketamine in concentrations of 0.5-2.0 mM led to a decrease in resting and stimulus-evoked activity. 7-Chlorokynurenic acid also blocked the responses to application of N-methyl-D-aspartate. The glyc ine agonist D-serine (0.01 mM) prevented the 7-chlorokynurenic inhibit ory effect. These results suggest the involvement of N-methyl-D-aspart ate receptors in mediating the actions of L-glutamate at the afferent synapses of the electroreceptor organs of the catfish. Copyright (C) 1 997 Published by Elsevier Science Ltd.